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Cryptotanshinone ameliorates renal ischaemia–reperfusion injury by inhibiting apoptosis and inflammatory response
Author(s) -
Bai Tao,
Yang Kang,
Qin Cong,
Xu Tao,
Yu Xi,
Zhang Jie
Publication year - 2019
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/bcpt.13275
Subject(s) - salvia miltiorrhiza , medicine , pharmacology , p38 mitogen activated protein kinases , apoptosis , renal injury , kidney , reperfusion injury , ischemia , mapk/erk pathway , acute kidney injury , kinase , chemistry , pathology , traditional chinese medicine , biochemistry , alternative medicine
Cryptotanshinone (CTS) is a natural compound from the Chinese herb Salvia miltiorrhiza . Previous studies demonstrated that CTS possesses anti‐apoptotic and anti‐inflammatory properties. However, its effects and underlying mechanism on renal ischaemia reperfusion (IR) injury remain unknown. In the present study, we investigated the effects of CTS on renal IR injury and its potential underlying mechanisms. Mice were randomized into four groups as follows: (a) sham operation + vehicle, (b) sham operation + CTS, (c) IR + vehicle, (d) IR + CTS. The CTS‐treated group were injected intraperitoneally with CTS (10 mg/kg/d) for 7 days prior to IR operation. Renal IR injury was induced by clamping the bilateral renal artery for 30 minutes followed by 24 hours of reperfusion. The mice were then killed to collect the serum and the kidneys for analysis. The results of the present study showed that CTS pretreatment significantly attenuates IR‐induced renal functional and morphological injuries, which was accompanied with inhibition of cell apoptosis and inflammatory response. Moreover, the phosphorylation of p38 mitogen‐activated protein kinase (MAPK) and the activation of nuclear factor‐κB (NF‐κB) signalling were inhibited by CTS. Therefore, CTS could be a useful therapeutic agent in the fight against renal IR injury.